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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Biased inheritance of the protein PatN frees vegetative cells to initiate patterned heterocyst differentiation
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Biased inheritance of the protein PatN frees vegetative cells to initiate patterned heterocyst differentiation

机译:蛋白质PatN的有偏遗传会释放营养细胞,从而启动模式化的异型囊肿分化

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摘要

Heterocysts, cells specialized for nitrogen fixation in certain filamentous cyanobacteria, appear singly in a nonrandom spacing pattern along the chain of vegetative cells. A two-stage, biased initiation and competitive resolution model has been proposed to explain the establishment of this spacing pattern. There is substantial evidence that competitive resolution of a subset of cells initiating differentiation occurs by interactions between a self-enhancing activator protein, HetR, and a diffusible pentapeptide inhibitor PatS-5 (RGSGR). Results presented here show that the absence of a unique membrane protein, PatN, in Nostoc punctiforme strain ATCC 29133 leads to a threefold increase in heterocyst frequency and a fourfold decrease in the vegetative cell interval between heterocysts. A PatN-GFP translational fusion shows a pattern of biased inheritance in daughter vegetative cells of ammonium-grown cultures. Inactivation of another heterocyst patterning gene, patA, is epistatic to inactivation of patN, and transcription of patA increases in a pat/V-deletion strain, implying that patN may function by modulating levels of patA. The presence of PatN is hypothesized to decrease the competency of a vegetative cell to initiate heterocyst differentiation, and the cellular concentration of PatN is dependent on cell division that results in cells transiently depleted of PatN. We suggest that biased inheritance of cell-fate determinants is a phylogenetic domain-spanning paradigm in the development of biological patterns.
机译:异质囊是专门用于某些丝状蓝细菌中固氮的细胞,仅沿着营养细胞链以非随机间隔模式出现。已经提出了一个两阶段,有偏差的起始和竞争解决模型来解释这种间隔模式的建立。有大量证据表明,通过自我增强的激活蛋白HetR和可扩散的五肽抑制剂PatS-5(RGSGR)之间的相互作用,可以发生细胞分化的竞争性竞争。此处显示的结果表明,在Nostoc点状菌株ATCC 29133中缺少独特的膜蛋白PatN会导致异型囊频率增加三倍,而异型囊之间的营养细胞间隔减少四倍。 PatN-GFP的翻译融合显示了铵态培养的子代营养细胞中遗传偏向的模式。另一个异型胞囊模式基因patA的失活与patN的失活相比是上位的,并且在pat / V缺失菌株中patA的转录增加,这意味着patN可能通过调节patA的水平发挥作用。假设存在PatN会降低营养细胞启动异型囊分化的能力,并且PatN的细胞浓度取决于细胞分裂,导致细胞瞬时耗尽PatN。我们建议细胞命运决定簇的有偏遗传是生物学模式发展中的系统发育域跨越范式。

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